SUMMARY OF PROPOSED OBJECTIVES: 1) Evaluation of the physiopharmacology of the efferent adrenergic neural-effector junctions involved in the production of pulmonary hypertension. a) To determine the effects of norepinephrine stimulation of pulmonary vascular effectors before and after (1) chemical blockade of alpha adrenergic receptors and (2) chemical denervation of the adrenergic nervous system. b) To determine the effects of dopamine stimulation of pulmonary vascular effectors before and after (1) chemical blackade of alpha adrenergic receptors, (2) chemical blockade of dopamine receptors and (3) chemical denervation of the adrenergic nervous system. d) To correlate the presence and absence of sympathetic adrenergic nerves in the lungs as demonstrated by catecholamine florescence techniques to the production of experimental pulmonary hypertension. e) To determine the extent to which lung plasma catecholamine levels can be altered by distention of the pulmonary artery wall. f) To compare the possible changes in lung plasma catecholamines produced by the pulmonary artery distention reflex to possible changes produced by stimulation of the stellate ganglion. g) To determine the extent that lung catecholamine turnover rates are altered by distention of the pulmonary artery wall. 2) Assessment of the possible mechanisms responsible for the arterial isocapnic hyperpnea produced as a consequence of the pulmonary artery balloon inflation. a) To assess the extent to which this isocapnic hyperpnea is a CO2 linked phenomenom. b) To investigate the possible reflex pathways and the nature of the receptors involved in the production of this hyperpnea. c) To demonstrate the extent to which the pattern of pulmonary blood flow is altered by balloon inflation within the main pulmonary artery. 3) Comparison of the production of pulmonary vasoconstriction by pulmonary artery wall distention to hypoxic pulmonary vasoconstriction. a) To demonstrate the normal pulmonary and systemic hemodynamic responses to acute hypoxia in the conscious non-sedated dog and compare these responses to those produced by balloon distention of the main pulmonary artery. b) To determine the extent that NE is involved in the production of the PH caused by acute hypoxia and balloon distention of the main pulmonary artery.